| Objective This study seeks to characterize the mechanism of delay wound healing in astreptozocin (STZ)-induced rat model of type Ⅰ diabetes mellitus (DM) and tounderstand the pathogenesis of diabetic keratopathy. Methods The rat model of DMwas induced via STZ injection in Sprague-Dawley rats. Body weight, length, andcorneal size were measured and compared with the age-matched normal controls.Corneal morphology was evaluated under digital confocal microscopy. Tear secretionwas measured with cotton threads, and corneal sensitivity was determined with anesthesiometer. Protein expression and distribution were assessed by Western blottingand immunohistochemistry. The process of corneal wound healing was observed bycorneal epithelial debridement model in vivo. The changes of permeability in corneaswounded after0hr,8hr,24hr,48hr,72hr and normal ones was detected. The remodelingof ZO-1and occludin in corneal epithelium cells was analyzed by an indirectimmunofluorescent technique in corneal wound healing process. Results Comparedwith the normal control rats, the body weight and length of Type Ⅰ DM rat induced bySTZ were significantly reduced (p<0.05), but no significant changes in corneal size andsurface. STZ rats showed stronger Rose Bengal staining (p<0.05), lesser tear secretingand innervation (p<0.05), and attenuated slightly sensitivity (p<0.05), more significantlydelayed corneal epithelial wound healing than that of normal control rats. Thephosphorylation of epidermal growth factor receptor （EGFR） was significantlydecreased in DM rat corneal epithelium, while tight junction proteins occludin andZO-1was unchanged, the remodeling of these tight junction proteins after woundclosure was delayed. Conclusions Corneal wound healing delay of type Ⅰ DM rats isrelated with decreasing EGFR signal transduction pathway and remolding of tightjunction protein ZO-1and occluding, meanwhile the decrease of tear secretion,impairment of innervation. |
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